Role of nitric oxide and nitrosative protein damage in cigarette smoke-induced emphysematous lung damage: Attenuation by vitamin C

Nitric Oxide ◽  
2012 ◽  
Vol 27 ◽  
pp. S41
Author(s):  
Indranil Gupta ◽  
Arijit Ghosh ◽  
Koustubh Panda
Keyword(s):  
Nitric Oxide ◽  
Vitamin C ◽  
Cigarette Smoke ◽  
Lung Damage ◽  
Protein Damage ◽  
Emphysematous Lung

scholarly journals Role of Oxidative Stress and Mitochondrial Dysfunction in Sepsis and Potential Therapies

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Konstantinos Mantzarlis ◽  
Vasiliki Tsolaki ◽  
Epaminondas Zakynthinos
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Intensive Care ◽  
Vitamin C ◽  
Causes Of Death ◽  
Redox Balance ◽  
Cardiac Performance ◽  
Efficiency Evaluation ◽  
Permeability Impairment

Sepsis is one of the most important causes of death in intensive care units. Despite the fact that sepsis pathogenesis remains obscure, there is increasing evidence that oxidants and antioxidants play a key role. The imbalance of the abovementioned substances in favor of oxidants is called oxidative stress, and it contributes to sepsis process. The most important consequences are vascular permeability impairment, decreased cardiac performance, and mitochondrial malfunction leading to impaired respiration. Nitric oxide is perhaps the most important and well-studied oxidant. Selenium, vitamin C, and 3N-acetylcysteine among others are potential therapies for the restoration of redox balance in sepsis. Results from recent studies are promising, but there is a need for more human studies in a clinical setting for safety and efficiency evaluation.

scholarly journals Cellular and molecular mechanisms of cigarette smoke-induced lung damage and prevention by vitamin C

2008 ◽  
Vol 5 (1) ◽  
pp. 21 ◽  
Author(s):  
Shuvojit Banerjee ◽  
Ranajoy Chattopadhyay ◽  
Arunava Ghosh ◽  
Hemanta Koley ◽  
Koustubh Panda ◽  
...  
Keyword(s):  
Vitamin C ◽  
Cigarette Smoke ◽  
Molecular Mechanisms ◽  
Lung Damage

scholarly journals Dendritic cells induce Tc1 cell differentiation via the CD40/CD40L pathway in mice after exposure to cigarette smoke

2016 ◽  
Vol 311 (3) ◽  
pp. L581-L589 ◽  
Author(s):  
Liang-Jian Kuang ◽  
Ting-Ting Deng ◽  
Qin Wang ◽  
Shi-Lin Qiu ◽  
Yi Liang ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Cell Differentiation ◽  
Cigarette Smoke ◽  
Lung Damage ◽  
Chronic Obstructive ◽  
Wild Type ◽  
Control Groups ◽  
Obstructive Pulmonary Disease

Dendritic cells and CD8+ T cells participate in the pathology of chronic obstructive pulmonary disease, including emphysema, but little is known of the involvement of the CD40/CD40L pathway. We investigated the role of the CD40/CD40L pathway in Tc1 cell differentiation induced by dendritic cells in a mouse model of emphysema, and in vitro. C57BL/6J wild-type and CD40−/− mice were exposed to cigarette smoke (CS) or not (control), for 24 wk. In vitro experiments involved wild-type and CD40−/− dendritic cells treated with CS extract (CSE) or not. Compared with the control groups, the CS mice (both wild type and CD40−/−) had a greater percentage of lung dendritic cells and higher levels of major histocompatability complex (MHC) class I molecules and costimulatory molecules CD40 and CD80. Relative to the CS CD40−/− mice, the CS wild type showed greater signs of lung damage and Tc1 cell differentiation. In vitro, the CSE-treated wild-type cells evidenced more cytokine release (IL-12/p70) and Tc1 cell differentiation than did the CSE-treated CD40−/− cells. Exposure to cigarette smoke increases the percentage of lung dendritic cells and promotes Tc1 cell differentiation via the CD40/CD40L pathway. Blocking the CD40/CD40L pathway may suppress development of emphysema in mice exposed to cigarette smoke.

The role of nitric oxide on cigarette smoke-induced programmed cell death in gastric mucosa

2000 ◽  
Vol 118 (4) ◽  
pp. A1141
Author(s):  
Hong-Ying Wang ◽  
Li Ma ◽  
Yang Li ◽  
Chi-Hin Cho
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Gastric Mucosa ◽  
Programmed Cell Death ◽  
Cigarette Smoke

scholarly journals Ascorbate attenuates pulmonary emphysema by inhibiting tobacco smoke and Rtp801-triggered lung protein modification and proteolysis

2016 ◽  
Vol 113 (29) ◽  
pp. E4208-E4217 ◽  
Author(s):  
Indranil Gupta ◽  
Souradipta Ganguly ◽  
Christine R. Rozanas ◽  
Dennis J. Stuehr ◽  
Koustubh Panda
Keyword(s):  
Lung Injury ◽  
Vitamin C ◽  
Tobacco Smoke ◽  
Protein Modification ◽  
Nitrosative Stress ◽  
Lung Damage ◽  
Cellular Damage ◽  
Protein Nitration ◽  
Human Lung Cells ◽  
Emphysematous Lung

Cigarette smoking causes emphysema, a fatal disease involving extensive structural and functional damage of the lung. Using a guinea pig model and human lung cells, we show that oxidant(s) present in tobacco smoke not only cause direct oxidative damage of lung proteins, contributing to the major share of lung injury, but also activate Rtp801, a key proinflammatory cellular factor involved in tobacco smoke-induced lung damage. Rtp801 triggers nuclear factor κB and consequent inducible NOS (iNOS)-mediated overproduction of NO, which in combination with excess superoxide produced during Rtp801 activation, contribute to increased oxido-nitrosative stress and lung protein nitration. However, lung-specific inhibition of iNOS with a iNOS-specific inhibitor, N6-(1-iminoethyl)-L-lysine, dihydrochloride (L-NIL) solely restricts lung protein nitration but fails to prevent or reverse the major tobacco smoke-induced oxidative lung injury. In comparison, the dietary antioxidant, ascorbate or vitamin C, can substantially prevent such damage by inhibiting both tobacco smoke-induced lung protein oxidation as well as activation of pulmonary Rtp801 and consequent iNOS/NO-induced nitration of lung proteins, that otherwise lead to increased proteolysis of such oxidized or nitrated proteins by endogenous lung proteases, resulting in emphysematous lung damage. Vitamin C also restricts the up-regulation of matrix-metalloproteinase-9, the major lung protease involved in the proteolysis of such modified lung proteins during tobacco smoke-induced emphysema. Overall, our findings implicate tobacco-smoke oxidant(s) as the primary etiopathogenic factor behind both the noncellular and cellular damage mechanisms governing emphysematous lung injury and demonstrate the potential of vitamin C to accomplish holistic prevention of such damage.

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